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Published on: February 5, 2015
Multiple sclerosis: cell-mediated immunity to human brain gangliosides
E Beraud1, M M Golstein, F Viallet
1Laboratoire d'Immunopathologie, Faculté de Médecine, Marseille.
Insights
Cell-mediated immunity (CMI) to gangliosides is heightened during Multiple Sclerosis (MS) attacks. Leukocyte Migration Inhibition (LMI) tests reveal increased hypersensitivity to these glycolipids in active MS patients.
Area of Science:
- Neuroimmunology
- Autoimmunity
Background:
- Cell-mediated immunity (CMI) to myelin components is implicated in Multiple Sclerosis (MS) pathogenesis.
- Gangliosides are a recently suggested target in MS, unlike Myelin Basic Protein with controversial findings.
Purpose of the Study:
- To investigate the involvement of gangliosides in MS pathogenesis.
- To assess cell-mediated immune response to human brain gangliosides in MS patients.
Main Methods:
- Leukocyte Migration Inhibition (LMI) tests were performed using human brain gangliosides.
- Participants included 39 MS patients (24 definite), 29 with Other Neurological Diseases (OND), 36 with Inflammatory Diseases (ID), and 40 healthy controls.
- MS patients were stratified by clinical stage (attack vs. no attack).
Main Results:
- The mean migration inhibition percentage in the MS-attack group was significantly higher (p < 0.01) compared to MS without attack, OND, ID, and healthy controls.
- Specifically, the MS-attack group showed 24.4 +/- 16.2% inhibition.
- LMI to gangliosides was significantly increased during the active MS attack stage.
Conclusions:
- These findings support the hypothesis of a Delayed Type Hypersensitivity (DTH) to gangliosides during active MS.
- CMI to gangliosides may play a role in the pathogenesis of Multiple Sclerosis during its active phase.
Abstract:
Cell-mediated immunity (CMI) to myelin components has been implicated in Multiple Sclerosis (MS) pathogenesis: two targets were suggested, Myelin Basic Protein with controversial results and, more recently, gangliosides. In order to investigate their possible involvement, we have performed Leukocyte Migration inhibition (LMI) tests in the presence of human brain gangliosides. Thirty nine MS patients (twenty four being "definite", according to McDonald and Halliday's classification), twenty nine patients with Other Neurological Diseases (OND), thirty six patients with Inflammatory diseases (ID) and forty healthy controls were tested. MS patients were divided into two groups, depending on the clinical stage of the disease. The mean migration inhibition percentage of the MS-attack group was found to be significantly different from the four others (p less than 0.01) (24.4 +/- 16.2 versus 10.9 +/- 8.5 in MS without attack, 4.4 +/- 12.9 in OND, 3.9 +/- 13.9 in ID and 11.1 +/- 12.1 in healthy subjects). LMI to gangliosides is therefore significantly increased during the attack stage in MS. These results support the notion of a Delayed Type Hypersensitivity to these glycolipids during the active stage of the disease.
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